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BACKGROUND: Optical penalization (OP) has previously been shown to successfully maintain vision in amblyopic eyes of older children when patching compliance is poor and when vision decreases once patching is discontinued. This study shows that the final vision in optically penalized eyes is often better than the vision obtained after patching alone. SUBJECTS AND METHODS: During the 5-year period from January 1992 to February 1997, 28 children aged between 3.7 and 8.2 years (average age, 6.5+/-1.1 years) were optically penalized for an average of 1.5+/-0.75 years. The maximum length of penalization was 3.3 years, whereas the minimum time was 6 months. There were 21 children with strabismic amblyopia and 7 children with anisometropic amblyopia. All 28 children had worn a patch to achieve their best visual levels and then had shown a loss of best vision when occlusion was stopped. Patching was usually resumed and continued until the previous best vision was obtained; at this point OP was started to "maintain" vision. Eighteen of the 28 children have discontinued penalization and have been followed up an average of 1(1/2) years. RESULTS: Twenty-six (93%) of the 28 patients showed an increase in best vision from that found at the conclusion of patching, and 2 patients maintained their vision at the initial level. The average visual acuity at the start of penalization was 20/50 (0.42+/-0.11 logarithm of the minimum angle of resolution [log MAR]). Final average visual acuity was 20/27 (0.15+/-0.12 log MAR). The average increase in vision was nearly 3 lines or 0.27+/-0.12 log MAR. CONCLUSION: OP alone (without the use of pharmacologic agents such as atropine) not only maintains vision after patching therapy, but also appears to improve the final visual outcome.  相似文献   
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目的:筛选一株优良的抗生素产生菌。方法:通过人为诱变来动摇产生菌原有的严密控制机制。结果:得到一种抗生素生物合成能力异常的突变株。结论:此方法可过量合成人们所期望的抗生素。  相似文献   
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目的:考察盐酸特拉唑嗪胶囊的稳定性。方法:通过影响因素(强光照射、高温、高温),加速和留样考察实验,以含量为测定指标,考察胶囊的含量变化。结果:在温度40℃、60℃、光照3500LX及RH75%等因素影响下,胶囊的含量无明显变化。结论:在25℃时,通过经典恒温加速试验推测盐酸特拉唑嗪胶囊的失效期为2年。  相似文献   
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AIM: To evaluate the nutritional status and its association with proinflammatory cytokines in children with chronic liver disease.METHODS: We performed a cross-sectional study with 43 children and adolescents, aged 0 to 17 years, diagnosed with chronic liver disease. All patients regularly attended the Pediatric Hepatology Unit and were under nutritional follow up. The exclusion criteria were fever from any etiology at the time of enrollment, inborn errors of the metabolism and any chronic illness. The severity of liver disease was assessed by Child-Pugh, Model for End-stage Liver Disease(MELD) and Pediatric End Stage Liver Disease(PELD) scores. Anthropometric parameters were height/age, body mass index/age and triceps skinfold/age according to World Health Organization standards. The cutoff points for nutritional status were risk of malnutrition(Z-score -1.00) and malnutrition(Z-score -2.00). Interleukin-1β(IL-1β), IL-6 and tumor necrosis factor-α levels were assessed by commercial ELISA kits. For multivariate analysis, linear regression was applied to assess the association between cytokine levels, disease severity and nutritional status. RESULTS: The median(25th-75 th centile) age of the study population was 60(17-116)-mo-old, and 53.5% were female. Biliary atresia was the main cause of chronic liver disease(72%). With respect to Child-Pugh score, cirrhotic patients were distributed as follows: 57.1% Child-Pugh A, a mild presentation of the disease, 34.3% Child-Pugh B, a moderate stage of cirrhosis and 8.6% Child-Pugh C, were considered severe cases. PELD and MELD scores were only above the cutoff point in 5 cases. IL-6 values were increased in patients at nutritional risk(34.9%) compared with those who were well-nourished [7.12(0.58-34.23) pg/m L vs 1.63(0.53-3.43) pg/m L; P = 0.02], correlating inversely with triceps skinfold-for-age z-score(rs =-0.61; P 0.001). IL-6 levels were associated with liver disease severity assessed by Child-Pugh score(P = 0.001). This association remained significant after adjusting for nutritional status in a linear regression model. CONCLUSION: High IL-6 levels were found in children with chronic liver disease at nutritional risk. Inflammatory activity may be related to nutritional status deterioration in these patients.  相似文献   
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ObjectiveInfant sleep problems can affect the child's health. Maternal characteristics have been associated with the quality of infant sleep, but few studies have investigated the impact of intrauterine conditions. The aim of the study was to evaluate the association between adverse intrauterine environments (maternal smoking, hypertension, diabetes, and intrauterine growth restriction) and extrauterine factors on infant sleep in the first 6 months of life.MethodsProspective cohort study, including singleton and at-term infants. Mothers were interviewed after delivery and at 30 days, 3 months, and 6 months of life. Socioeconomic, breastfeeding, and sleep data were self-reported by mothers using semi-structured interviews. Maternal stress (Perceived Stress Scale) and postpartum depression symptoms (Edinburgh Postpartum Depression Scale) were assessed.ResultsThere was no statistically significant association between intrauterine environments and the sleep of infants of the 359 mother–child dyads investigated. Total infant sleep time decreased from approximately 13–11 h from 30 days to 6 months of age (p < 0.001) and the longest period of uninterrupted sleep increased from approximately 4–6 h during the same period (p < 0.001). Breastfed infants slept longer in 24-h periods in the first month, but they woke up more often throughout the night when compared to infants receiving formula. Mothers with depressive symptoms reported increased sleep latency time.ConclusionsAdverse intrauterine environments did not significantly affect sleep measures in the first 6 months of life. Maternal characteristics and practices, however, were associated with infant sleep, suggesting that environmental factors significantly contribute to sleep quality early in life.  相似文献   
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Schwann cells are glial cells of peripheral nervous system, responsible for axonal myelination and ensheathing, as well as tissue repair following a peripheral nervous system injury. They are one of several cell types that are widely studied and most commonly used for cell transplantation to treat spinal cord injury, due to their intrinsic characteristics including the ability to secrete a variety of neurotrophic factors. This mini review summarizes the recent findings of endogenous Schwann cells after spinal cord injury and discusses their role in tissue repair and axonal regeneration. After spinal cord injury, numerous endogenous Schwann cells migrate into the lesion site from the nerve roots, involving in the construction of newly formed repaired tissue and axonal myelination. These invading Schwann cells also can move a long distance away from the injury site both rostrally and caudally. In addition, Schwann cells can be induced to migrate by minimal insults (such as scar ablation) within the spinal cord and integrate with astrocytes under certain circumstances. More importantly, the host Schwann cells can be induced to migrate into spinal cord by transplantation of different cell types, such as exogenous Schwann cells, olfactory ensheathing cells, and bone marrow-derived stromal stem cells. Migration of endogenous Schwann cells following spinal cord injury is a common natural phenomenon found both in animal and human, and the myelination by Schwann cells has been examined effective in signal conduction electrophysiologically. Therefore, if the inherent properties of endogenous Schwann cells could be developed and utilized, it would offer a new avenue for the restoration of injured spinal cord.  相似文献   
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